NCLEX-RN · Physiological Adaptation · 7 min read
Acute Kidney Injury and Dialysis
- Differentiate the etiologies, pathophysiology, and clinical phases of acute kidney injury to anticipate fluid, electrolyte, and acid-base imbalances.
- Formulate nursing interventions for patients undergoing hemodialysis, including vascular access protection, medication scheduling, and the management of acute dialysis emergencies.
- Apply safe nursing practices for peritoneal dialysis management, recognizing complications such as peritonitis, bowel perforation, and respiratory compromise.
Etiologies and Mechanisms of Acute Kidney Injury
Acute kidney injury is characterized by a rapid decline in renal function, which leads to the accumulation of nitrogenous waste products in the blood. When assessing kidney function, serum creatinine is generally more specific for kidney filtration than blood urea nitrogen, but serum creatinine can lag behind an acute decline in kidney function. To systematically evaluate the underlying cause of acute kidney injury, clinicians classify the condition into three distinct categories based on anatomical location: prerenal, intrarenal, and postrenal.
Prerenal acute kidney injury is caused by decreased renal blood flow and perfusion. This hypoperfusion often results from systemic conditions such as hypovolemia, sepsis, shock, or heart failure. In these situations, the kidney tissue itself remains initially intact, but it receives inadequate blood flow to support normal glomerular filtration. Postrenal acute kidney injury, in contrast, occurs distal to the renal parenchyma and is caused by mechanical obstruction of urinary outflow. Common causes of postrenal obstruction include benign prostatic hyperplasia, calculi, or tumors. When urine cannot leave the kidneys due to a physical blockage, retrograde pressure builds up and impairs ongoing renal function.
Intrarenal acute kidney injury results from direct damage to renal tissue. Ischemia and nephrotoxic medications are frequent triggers of acute tubular injury. Aminoglycoside antibiotics can cause nephrotoxic intrarenal injury, and intravenous iodinated contrast may also contribute to acute kidney injury, particularly in patients with pre-existing risk factors. Nonsteroidal anti-inflammatory drugs commonly cause prerenal (hemodynamic) acute kidney injury by inhibiting renal prostaglandins and constricting afferent arterioles; they can also cause intrarenal injury, such as acute interstitial nephritis. In addition, rhabdomyolysis causes intrarenal acute kidney injury secondary to renal tubular obstruction and direct toxicity from circulating myoglobin.
| Classification | Primary Mechanism | Common Etiologies |
|---|---|---|
| Prerenal | Decreased renal blood flow and perfusion | Hypovolemia, sepsis, shock, heart failure |
| Intrarenal | Direct damage to renal tissue and acute tubular injury | Ischemia, aminoglycoside antibiotics, intravenous iodinated contrast, nonsteroidal anti-inflammatory drugs, rhabdomyolysis |
| Postrenal | Mechanical obstruction of urinary outflow | Benign prostatic hyperplasia, calculi, tumors |
Common mistakes
- Assuming that holding all antihypertensive medications prior to hemodialysis is standard procedure, rather than individualizing timing based on blood pressure, the medication, and the dialysis prescription with a provider order.
- Using a microwave oven to heat peritoneal dialysate instead of an approved dry-heat warmer, which risks uneven heating and patient injury.
- Failing to recognize that dialysate effluent appearance provides vital diagnostic clues, such as cloudy fluid indicating peritonitis or brown/feculent fluid indicating bowel perforation.
- Assuming dietary protein restrictions for non-dialyzed kidney disease apply equally to peritoneal dialysis, overlooking that peritoneal dialysis causes significant dialysate protein loss that necessitates higher dietary protein intake.
Key points
- Acute kidney injury is classified as prerenal (hypoperfusion), intrarenal (renal tissue injury, such as acute tubular injury from ischemia or nephrotoxins), or postrenal (urinary outflow obstruction); NSAIDs commonly cause hemodynamic, prerenal acute kidney injury through afferent arteriolar constriction, although they can also cause intrarenal injury such as acute interstitial nephritis.
- The oliguric phase (<400 mL/day) creates risks of fluid overload, metabolic acidosis, and hyperkalemia; hyperkalemia with electrocardiographic changes requires immediate cardiac stabilization with intravenous calcium, rapid intracellular shifting with treatments such as insulin with dextrose, and assessment for definitive potassium removal, including dialysis when indicated.
- The diuretic phase brings increased urine output but carries risks of hypovolemia, hypotension, dehydration, hypokalemia, and hyponatremia; daily morning weight on the same scale remains the single most accurate indicator of fluid shifts.
- Arteriovenous fistula or graft patency is verified by a continuous thrill and bruit; venipunctures, IV insertions, and blood pressure readings are strictly contraindicated in the access extremity, and distal hypoperfusion warrants assessment for arterial steal syndrome.
- Hemodialysis complications include hypotension (treated with reduced ultrafiltration and isotonic saline), disequilibrium syndrome (prevented by lower blood flow rates and shorter initial sessions), and air embolism (managed by stopping the blood pump, clamping the venous line, left-side positioning with the head lowered, and high-flow oxygen).
- Peritoneal dialysis requires strict aseptic technique and mask-wearing by both patient and nurse; complications include peritonitis (heralded by cloudy effluent and abdominal pain), bowel perforation (brown/feculent effluent), and respiratory compromise (relieved by semi-Fowler positioning).
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Sample lesson: Fluid, Electrolyte and Acid-Base Imbalances25 practice questions on this exam
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